Evidence map›Paper›PMID 20974973›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Identification of a receptor for an extinct virus.

Steven J Soll, Stuart J D Neil, Paul D Bieniasz

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. The human endogenous retroviral envelope HEMO protein interacts with BACE2: Novel partnership acquired in the primate lineage.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Article
  3. Review
  4. Convergent evolution of antiviral machinery derived from endogenous retrovirus truncated envelope genes in multiple species.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Pushing the endogenous envelope.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2013
    Review
  14. Review
  15. Host genes important to HIV replication and evolution.Cold Spring Harbor perspectives in medicine · 2012
    Review
  16. Review
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 2 countries.

Steven J SollThe Howard Hughes Medical Institute, The Aaron Diamond AIDS Research Center, The Rockefeller University, New York, NY 10016, USA.
Stuart J D Neil
Paul D Bieniasz
Aaron Diamond AIDS Research Center · USKing's College London · GBRockefeller University · US

Funding

Retrovirus Restriction by Trima5alphaR01AI064003 · NIAID · AARON DIAMOND AIDS RESEARCH CENTER · PI BIENIASZ, PAUL D. · 2005 to 2009
$2.1M
Howard Hughes Medical InstituteNIAID NIH HHS R01 AI064003NIAID NIH HHS R01 AI64003
6 · The paper itself

Abstract

The resurrection of endogenous retroviruses from inactive molecular fossils has allowed the investigation of interactions between extinct pathogens and their hosts that occurred millions of years ago. Two such paleoviruses, chimpanzee endogenous retrovirus-1 and -2 (CERV1 and CERV2), are relatives of modern MLVs and are found in the genomes of a variety of Old World primates, but are absent from the human genome. No extant CERV1 and -2 proviruses are known to encode functional proteins. To investigate the host range restriction of these viruses, we attempted to reconstruct functional envelopes by generating consensus genes and proteins. CERV1 and -2 enveloped MLV particles infected cell lines from a range of mammalian species. Using CERV2 Env-pseudotyped MLV reporters, we identified copper transport protein 1 (CTR1) as a receptor that was presumably used by CERV2 during its ancient exogenous replication in primates. Expression of human CTR1 was sufficient to confer CERV2 permissiveness on otherwise resistant hamster cells, and CTR1 knockdown or CuCl(2) treatment specifically inhibited CERV2 infection of human cells. Mutations in highly conserved CTR1 residues that have rendered hamster cells resistant to CERV2 include a unique deletion in a copper-binding motif. These CERV2 receptor-inactivating mutations in hamster CTR1 are accompanied by apparently compensating changes, including an increased number of extracellular copper-coordinating residues, and this may represent an evolutionary barrier to the acquisition of CERV2 resistance in primates.

Indexed as

Extinction, BiologicalAnimalsCation Transport ProteinsCopper Transporter 1CricetinaeEndogenous RetrovirusesHumansMolecular Sequence DataPan troglodytesReceptors, VirusVirusesCation Transport ProteinsCopper Transporter 1Receptors, VirusSLC31A1 protein, human

Identifiers

PMID20974973
PMCPMC2984158
OpenAlexW1997799310

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.